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羧甲基纤维素可促进兔角膜上皮伤口愈合。

Carboxymethyl cellulose stimulates rabbit corneal epithelial wound healing.

作者信息

Garrett Qian, Xu Shunjiang, Simmons Peter A, Vehige Joseph, Xie Ruo Zhong, Kumar Ajay, Flanagan Judith L, Zhao Zhenjun, Willcox Mark D P

机构信息

Institute for Eye Research, Sydney, New South Wales, Australia.

出版信息

Curr Eye Res. 2008 Jul;33(7):567-73. doi: 10.1080/02713680802140213.

DOI:10.1080/02713680802140213
PMID:18600489
Abstract

PURPOSE

Previously, we reported carboxymethyl cellulose (CMC) binding to human corneal epithelial cells and promoting corneal epithelial wound closure in vitro. Using an animal model, the efficacy of CMC in promoting corneal wound healing was examined.

MATERIALS AND METHODS

Following corneal epithelial wounding of NZ white rabbits, CMC (0.2% or 1.0%) or control vehicle (PBS) was administered topically (4 times daily for 3 days) to wounded and unwounded eyes with or without contact lens wear. Wound healing in response to the treatments was measured as percentage reduction of fluorescein-stained wound area 0 to 72 hr post-wounding. Corneas were examined histologically and expression of zonula occludens-1 (ZO-1) tight-junction was detected by immunohistochemistry.

RESULTS

Percentage wound reduction in CMC-treated groups was significantly greater than controls (p < 0.05) at 24 and 32 hr. Complete wound closure was observed by 48 hr in 100% of CMC-treated eyes compared to 45% of vehicle-treated eyes. CMC also promoted wound closure dose-dependently. Epithelial cells formed an intact layer following CMC-treatment whereas vehicle-treated cells were less ordered. Strong ZO-1 expression in corneal epithelia of CMC-treated eyes was observed at 72 hr. Contact lens wear appeared to delay wound closure compared to without lens wear during CMC-treatment (p = 0.001).

CONCLUSIONS

CMC promoted dose-dependent corneal epithelial wound healing. CMC stimulated ZO-1 expression, indicating accelerated corneal epithelial resistance barrier regeneration.

摘要

目的

此前,我们报道了羧甲基纤维素(CMC)与人角膜上皮细胞结合并在体外促进角膜上皮伤口闭合。使用动物模型,研究了CMC在促进角膜伤口愈合方面的功效。

材料与方法

对新西兰白兔进行角膜上皮损伤后,将CMC(0.2%或1.0%)或对照载体(PBS)局部应用于受伤和未受伤的眼睛(每天4次,共3天),无论是否佩戴隐形眼镜。在受伤后0至72小时,通过测量荧光素染色伤口面积的减少百分比来评估治疗后的伤口愈合情况。对角膜进行组织学检查,并通过免疫组织化学检测紧密连接蛋白-1(ZO-1)的表达。

结果

在24小时和32小时时,CMC治疗组的伤口减少百分比显著高于对照组(p<0.05)。在48小时时,100%接受CMC治疗的眼睛实现了完全伤口闭合,而接受载体治疗的眼睛这一比例为45%。CMC还呈剂量依赖性地促进伤口闭合。CMC治疗后上皮细胞形成完整层,而载体治疗的细胞排列较无序。在72小时时,观察到CMC治疗的眼睛角膜上皮中ZO-1表达强烈。与CMC治疗期间不佩戴隐形眼镜相比,佩戴隐形眼镜似乎延迟了伤口闭合(p = 0.001)。

结论

CMC促进了剂量依赖性的角膜上皮伤口愈合。CMC刺激了ZO-1表达,表明角膜上皮抵抗屏障再生加速。

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